Targeted deletion of MMP-9 attenuates myocardial contractile dysfunction in heart failure

Physiological Research

Volumn 57, Issue 3, 2008, Pages 379-384

  Moshal, K S ^a   Rodriguez, W E ^a   Sen, U ^a   Tyagi, Suresh C ^a  

^a University of Louisville School of Medicine   (United States)

Author keywords

Aortocaval shunt; Endothelial myocyte uncoupling; LV rings; Ventricular contraction; Volume overload

Indexed keywords

ACETYLCHOLINE; BRADYKININ; GELATINASE B; MMP9 PROTEIN, MOUSE; NITROPRUSSIDE SODIUM;

ANIMAL; ARTERIOVENOUS SHUNT; ARTICLE; DISEASE MODEL; DOSE RESPONSE; DRUG EFFECT; ENDOTHELIUM CELL; ENZYME ACTIVATION; ENZYMOLOGY; GENETICS; HEART CONTRACTION; HEART FAILURE; HEART LEFT VENTRICLE FUNCTION; HEART MUSCLE; HEART VENTRICLE; MALE; METABOLISM; MOUSE; MOUSE MUTANT; PATHOPHYSIOLOGY; PHENOTYPE;

ACETYLCHOLINE; ANIMALS; ARTERIOVENOUS SHUNT, SURGICAL; BRADYKININ; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ENDOTHELIAL CELLS; ENZYME ACTIVATION; HEART FAILURE; HEART VENTRICLES; MALE; MATRIX METALLOPROTEINASE 9; MICE; MICE, KNOCKOUT; MYOCARDIAL CONTRACTION; MYOCARDIUM; NITROPRUSSIDE; PHENOTYPE; VENTRICULAR FUNCTION, LEFT;

EID: 45849089609     PISSN: 08628408     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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